e arginine) or mutant (ie glutamine or histidine) In

e. arginine) or mutant (i.e. glutamine or histidine). In MG-132 purchase addition, substitutions at amino acids 2290–2248 of the NS5A region (interferon-sensitivity determining region) were determined as described previously.[31] Amino acid substitutions in this region were defined as wild type (0 or 1) or non-wild type (≥2). Genomic DNA was extracted from whole blood using the MagNA Pure LC and a DNA Isolation Kit (Roche Diagnostics). The genetic polymorphism near the interleukin-28B (IL28B) gene,[32, 33] rs8099917, was genotyped by real-time PCR

using the TaqMan SNP Genotyping Assays and the 7500 Fast Real-Time PCR System (Applied Biosystems, Foster City, CA, USA). The rs8099917 genotypes were classified as TT (major genotype) or non-TT (minor genotype: TG or GG). Continuous variables are expressed as means and standard deviations. Continuous data were analyzed using the non-parametric Mann–Whitney U-test. Categorical data were analyzed using the χ2-test with a Yates correction or Fisher’s exact test. Univariate and multivariate

logistic regression analyses were performed to identify factors that significantly contributed to SVR. Odds ratios (OR) and 95% confidence intervals (95% CI) were also calculated. All P-values for statistical tests were two-tailed. The levels of significance and marginal significance were set at P < 0.05 and P < 0.15, respectively. Variables showing statistical or marginal significance in univariate analysis were entered into multivariate SB203580 mw logistic regression analyses to identify significant independent predictive factors of SVR. All statistical analyses were performed using SPSS version 17.0 (IBM-SPSS, Chicago, IL, USA). In this study, the adherence to each drug was excluded for the difference of treatment duration and the stopping rules. PATIENT CHARACTERISTICS ARE summarized in Table 1. Of the

103 patients, 57 (55.3%) and 46 (44.7%) were partial and null responders, respectively. Partial responders had significantly higher platelet counts than null responders (P = 0.0126). α-Fetoprotein levels were significantly lower in partial responders than null responders (P = 0.0202). No other baseline factors differed significantly between groups. Regarding treatment outcomes of TVR-based triple combination therapy, 58 patients (56.3%) achieved SVR, 23 (22.3%) showed relapse, 16 (15.5%) Rolziracetam showed VBT and six (5.8%) showed non-response. Patients were stratified according to previous treatment response and regimen. Among the 50 partial responders treated with T12PR24, 35 (70.0%) achieved SVR, 12 (24.0%) showed relapse and three (6.0%) showed VBT. Among the seven partial responders treated with T12PR48, six (85.7%) achieved SVR and one (14.3%) showed VBT. Among all partial responders, the SVR rate was slightly higher with T12PR48 than T12PR24 (6/7 [85.7%] vs 35/50 patients [70.0%]), though not statistically significant (P = 0.6763) (Fig. 1).

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